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A gls24 disruption mutant has also been shown to be highly attenuated in animal infection models [58], [59].
Moreover, a Salmonella SPI-1 mutant has also been shown to preferentially target and invade mouse epithelial M cells and polarized epithelial cells cultured under conditions that allow them to express M-cell like phenotypes, phenotypes that include particle uptake and transportation of antigens [16], [39], [41], [50], [51], [52], [53], [54].
Finally, a L77A/L91A double mutant has also been included in this study.
However, overexpression of the catalytically inert mutant has also a relatively minor effect on the integrity of DNA MMR.
This offered the possibility that, with this acquired enzymatic activity, the LW mutant has also acquired the ability to act as a presynaptically neurotoxic sPLA2.
Moreover, in addition to abrogating the tumor suppressor functions of wild-type TP53, R273H mutant has also been found to acquire new oncogenic activities to promote cancer, including metastasis promotion and increased resistance to anticancer treatments [ 42, 43].
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In mice implanted with pancreatic tumors, intratumoral injections of an adenovirus expressing the Rac1T17N mutant have also led to significant tumor growth inhibitions.
The involvement of different phytohormones (ethylene, jasmonate, salicylic acid) in modulating the singlet oxygen-mediated cell death during stress in Arabidopsis mutants has also been demonstrated earlier (Danon et al. 2005, Ochsenbein et al. 2006).
Investigation of Creb/Atf1 subfamily mouse mutants has also revealed that Creb/Atf1 subfamily members may compensate for one another.
Relaxation of (positive) interference in meiotic mutants has also been observed, despite a general tendency toward linkage tightening [ 67– 67].
Electron microscopy of Sec16 mutants has also shown an absence of the distinct 40 80 nm COPII transport vesicles (Kaiser and Schekman 1990).
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